Neurocognitive syndrome of “long covid”: literature review

Uvod: Iako je SARS-CoV-2 respiratorna infekcija, virus je neurotropan i 40% bolesnika ima neurološke manifestacije. Česta pojava slučajeva sa produženim smetnjama posle COVID-19 nametnula je uvođenje sindroma „dugog COVID-a”, koji označava set različitih simptoma koji perzistiraju minimum četiri nedelje nakon akutne infekcije. Jedna od vodećih manifestacija je kognitivni pad. Cilj: Analiza učestalosti i neuropsihološkog profila kognitivnog pada u „dugom COVID-u”. Metod: Pregled literature. Rezultati: Među CNS posledicama „dugog COVID-a” najčešće se registruju kognitivni pad, glavobolja, izmene sna i vrtoglavica. Kognitivne izmene bolesnici opisuju kao doživljaj postojanja „magle u glavi”, a podrazumeva pad koncentracije ili smetnje kratkoročnog pamćenja, koji može da utiče na povratak uobičajenom socijalnom i profesionalnom funkcionisanju. Neurokognitivne komplikacije akutne SARS-CoV-2 infekcije se opisuju naročito kod kritično obolelih i respiratorno ugroženih bolesnika i porede sa sličnim sindromima posle sepse ili boravka u jedinicama intenzivnog lečenja („post-ICU syndrome“). Međutim, bar 20% bolesnika sa blagim formama COVID-19 koje nisu zahtevale hospitalizaciju takođe ima produžene kognitivne smetnje. Fenomeni u sklopu „brain fog“ slični su onima kod osoba sa sindromom hroničnog umora. Infekcija SARS-Cov-2 virusom bilo kog stepena težine povećava rizik za nastanak kognitivnog pada. Do sada nije istražen uticaj kognitivnog pada nakon COVID-19 na kvalitet života i aktivnosti svakodnevnog življenja, kao i uticaj psiholoških i socijalnih aspekata pandemije na kogniciju. Mogući mehanizmi kognitivne disfukcije su: direktna infekcija CNS-a, udaljeni efekti sistemske infekcije („citokinska oluja” i dr.), vaskularno oštećenje mozga, neuroinflamacija, autoimuni odgovor protiv CNS-a, hipometabolizam limbičkog sistema i orbitofrontalnog korteksa, kao i neurodegeneracija slična onoj u Alchajmerovoj bolesti, pri čemu je moguće da se neki od ovih mehanizama prepliću. Zaključak: Kognitive manifestacije „dugog COVID-a” nisu retke i značajno utiču na povratak u uobičajeni lični i profesionalni milje preživelih. Neophodno je dugoročno praćenje ovih bolesnika i sagledavanje različitih etioloških i terapijskih aspekata kognitivnih izmena u okviru „dugog COVID-a”.Introduction: Although SARS-CoV-2 is a respiratory infection, the virus is neurotropic and neurological manifestations are seen in 40% patients. Recognition of prolonged post-COVID symptoms led to the introduction of the term “long COVID syndrome”, referring to a set of various symptoms persisting for a minimum of four weeks after acute infection. One of the main manifestations is cognitive decline. Aim: Analysis of incidence and neuropsychological profile of cognitive decline in “long COVID” syndrome. Method: Literature review. Results: Most frequent CNS manifestations of “long COVID” include cognitive decline, headache, sleep disturbance, and dizziness. Cognitive changes are reported as “brain fog” and correspond to a decline in attention and short-term memory, impacting return to premorbid social and professional activities. Acute SARS-CoV-2 neurocognitive complications are seen particularly in critically ill and respiratory insufficient patients, comparable to the similar phenomenon of post-sepsis and intensive care unit treatment (“post-ICU syndrome”). However, 20% of patients with mild COVID-19, not requiring hospitalization, also reported prolonged cognitive complaints, resembling those in patients with chronic fatigue syndrome. SARS-Cov-2 infection of any severity increases the risk for cognitive decline. The impact of post-COVID cognitive decline on the quality of life and activities of daily living as well as the influence of psychological and social aspects of the pandemic on cognition remain to be investigated. Potential mechanisms of cognitive dysfunction are direct CNS infection, remote effects of systemic infection (“cytokine storm” etc.), vascular brain damage, neuroinflammation, autoimmune response directed to the CNS components, hypometabolism in the limbic and orbitofrontal cortex, as well as neurodegeneration comparable to those in Alzheimer’s disease. Several different mechanisms may also be intertwined. Conclusion: Cognitive manifestations of “long COVID” are not rare and have a significant influence on personal and professional activities of the survivors. Long-term follow-up and analysis of various etiological and therapeutic aspects of cognitive changes within “long-COVID” are needed